TENT5C and gastroesophageal reflux disease: Its downregulation, as suggested by our data, might lead to impaired stability of transcripts encoding for epithelial junction proteins or cytoprotective factors, thereby rendering the mucosa more susceptible to acid-peptic injury.[58] Furthermore, FAM46C has been demonstrated to inhibit autophagy and promote the accumulation of protein aggregates, exacerbating ER stress.[59,60] Given that ER stress is a known mechanism in GERD pathogenesis,[7] loss of FAM46C function could amplify this stress response, leading to enhanced epithelial cell damage and impaired healing.